Profuse Watery Diarrhea Research Articles

Heat-Labile Toxin from Enterotoxigenic Escherichia coli Causes Systemic Impairment in Zebrafish Model.

Heat-labile toxin I (LT-I), produced by strains of enterotoxigenic Escherichia coli (ETEC), causes profuse watery diarrhea in humans. Different in vitro and in vivo models have already elucidated the mechanism of action of this toxin; however, their use does not always allow for more specific studies on how the LT-I toxin acts in systemic tracts and intestinal cell lines. In the present work, zebrafish (Danio rerio) and human intestinal cells (Caco-2) were used as models to study the toxin LT-I. Caco-2 cells were used, in the 62nd passage, at different cell concentrations. LT-I was conjugated to FITC to visualize its transport in cells, as well as microinjected into the caudal vein of zebrafish larvae, in order to investigate its effects on survival, systemic traffic, and morphological formation. The internalization of LT-I was visualized in 3 × 104 Caco-2 cells, being associated with the cell membrane and nucleus. The systemic traffic of LT-I in zebrafish larvae showed its presence in the cardiac cavity, yolk, and regions of the intestine, as demonstrated by cardiac edema (100%), the absence of a swimming bladder (100%), and yolk edema (80%), in addition to growth limitation in the larvae, compared to the control group. There was a reduction in heart rate during the assessment of larval survival kinetics, demonstrating the cardiotoxic effect of LT-I. Thus, in this study, we provide essential new depictions of the features of LT-I.

Life-Threatening VIPoma Crisis in an Immunocompromised Patient

Background: Vasoactive intestinal peptide-secreting tumors (VIPoma) are rare neuroendocrine tumors (NETs) that present with a triad of profuse watery diarrhea, hypokalemia, and achlorhydria. The resulting renal impairment, electrolytes and acid-base imbalances pose a high risk of morbidity and mortality. We describe a case of life-threatening VIPoma crisis in an immunocompromised patient. Clinical Case: A 64-year-old man was intubated after he was brought in unconscious with tachypnea. Upon review, he had experienced persistent watery diarrhea for the past 6 months, with a weight loss of 18 kg. He had severe hypokalemia (potassium 1.9 mmol/L, n= 3.5-5.0), metabolic acidosis (blood gases pH 6.927, bicarbonate 4.8 mmol/L, base excess -25.9 mmol/L), and acute kidney injury (urea 47.9 mmol/L, creatinine 980umol/L). He continued to have electrolyte imbalances and acidosis due to persistent diarrhea, despite hydration and dialysis support. His biohazard screening results were positive for human immunodeficiency virus (HIV), with a CD4 count of 101 cells/µl. He was given courses of antibiotics for treating pathogenic infections; however, his septic workups were negative for infection, including HIV-related opportunistic infections. Later, pancreatic CT revealed a well-defined heterogeneously enhancing pancreatic head mass, size 6.8x5.2x7.5 cm. Further laboratory investigations confirmed the diagnosis of VIPoma, with elevated VIP levels (1600 pg/ml, n < 75). Eventually, subcutaneous octreotide was started, with resolution of the diarrhea and normalization of his electrolytes and renal function. After a 6-week hospital stay, he was discharged well with monthly octreotide and initiated on antiretroviral therapy (ART). After 3 months of ART, his CD4 count improved, and he remained diarrhea-free with octreotide. He is scheduled for tumor debulking surgery. Conclusion:This case highlights the importance of having a clinical suspicion of NETs, especially in immunocompromised patients. Further investigations and imaging studies to rule out noninfectious pathologies should be considered in patients who respond poorly to standard therapy. In VIPoma, somatostatin analog is an antisecretory treatment and it is highly effective for controlling diarrhea. High-dose octreotide up to 1500 µg/day has previously been studied for treatment of refractory diarrhoea in the setting of HIV infection² and it has been found to be helpful in reducing stool volume and frequency. Lastly, delays in the diagnosis and treatment of VIPoma in immunocompromised patients can be fatal. References1/ Hoffland J., Kaltsas G., de Herder W. Advances in the Diagnosis and Management of Well-Differentiated Neuroendocrine Neoplasms. Endocrine Reviews, Volume 41, Issue 2, April 2020, Pages 371-403.2/ Farthing MJ. Octreotide in the treatment of refractory diarrhoea and intestinal fistulae. Gut 1994;35:S5-10.

Levodopa/dopa decarboxylase inhibitor associated microscopic colitis: An under-recognized drug reaction

BackgroundMicroscopic colitis is a form of inflammatory bowel disease characterized by profuse non-bloody watery diarrhea. Macroscopic abnormality is not present on colonoscopy, and it requires biopsy for diagnosis. Few cases have been attributed to levodopa/dopa-decarboxylase inhibitor therapy. MethodA retrospective cohort study of 21 patients on levodopa/benserazide and one patient on levodopa-carbidopa intestinal gel with clinically suspected or biopsy proven microscopic colitis. ResultsAll 21 patients on oral levodopa/benserazide had resolution of diarrhea with cessation of the medication. Four patients discontinued levodopa permanently. Two were rechallenged with levodopa/benserazide without symptom recurrence. One patient on oral levodopa/carbidopa developed diarrhea only with intermittent dispersible levodopa/benserazide. 14 were switched to levodopa/carbidopa with resolution of diarrhea in 9 but symptom recurrence in 5. One patient on oral levodopa/benserazide developed profuse diarrhea when switched to levodopa-carbidopa intestinal gel. Of 7/22 patients who had colonoscopy and biopsy, 5 had histopathological proven microscopic colitis. Conclusionlevodopa/dopa-decarboxylase inhibitor induced microscopic colitis may be more common than previously suspected, with the potential to affect treatment compliance and therapeutic options.

Rotavirus gastroenteritis as a precipitating factor of celiac crisis in infancy: Case reports and review of literature

Introduction. Celiac crisis is a rare and life-threatening complication of celiac disease. Although it occurs in all ages, the most common affects children within the first two years. Outline of cases. We report three infants (two female, one male, age range 9?12) with celiac crises as an initial presentation of celiac disease precipitated with rotavirus gastroenteritis. Celiac crisis was preceded by failure to thrive caused by anorexia, occasional vomiting and frequent abundant stools for 4?8 weeks, and 1?2 days before admission with fever, frequent vomiting and profuse watery diarrhea. They were admitted in a very severe general condition, severely dehydrated, markedly malnourished, with an enormously distended abdomen, edema of the lower legs and feet, and perianal erythema. After correction of dehydration and hypoalbuminemia, they were placed on a gluten- and disaccharide-free diet and within the first two weeks on additional parenteral nutrition. The applied therapeutic measures resulted in stabilization and further rapid improvement of the patient?s condition. In all three patients the latex agglutination test for rotavirus was positive, IgA anti-TTG antibodies elevated (58.6?78 U/ml) and all three were homozygous carriers of the HLA DQ2 gene. Enterobiopsy was performed two weeks after the admission and total villous atrophy (Marsh IIIc) was registered in all three patients. In the further course, the complete recovery of the patient was accomplished by a strict gluten-free diet. Conclusion. Our experience indicates that rotavirus gastroenteritis in timely unrecognized classical celiac disease in infants can lead to celiac crisis.

Cryptosporidium Infections in Africa-How Important Is Zoonotic Transmission? A Review of the Evidence.

Cryptosporidium, a protozoan parasite in the phylum Apicomplexa, is the etiological agent of cryptosporidiosis, an intestinal infection characterized by profuse watery diarrhea. Over 30 species of Cryptosporidium are recognized, some host specific whereas others infect a broader host range. Cryptosporidium hominis and Cryptosporidium parvum are the species most commonly associated with human infection; C. hominis is largely associated only with human infections, but C. parvum is also associated with infection in animals, especially young ruminants. In some regions, cryptosporidiosis is a serious veterinary problem, particularly for calves, and lambs. Many outbreaks of human cryptosporidiosis have been associated with zoonotic transmission following contact with infected animals. In Africa, where cryptosporidiosis is a major contributor to pediatric morbidity and mortality, evidence suggests transmission is principally anthroponotic. Given the frequent close contact between humans and animals in Africa, the apparent predominance of human-to-human transmission is both interesting and puzzling. In this article, after a brief “text book” introduction to the parasite, we consider in separate sections the different aspects of relevance to Cryptosporidium transmission in African countries, describing different aspects of the various species and subtypes in human and animal infections, considering livestock management practices in different African countries, and looking for any characteristic “hot spots” where zoonotic transmission has apparently occurred. Studies where transmission networks have been investigated are particularly relevant. Finally, in a separate section, we try to gather these different strands of evidence together in order to assess the reasons behind the apparent predominance of anthroponotic transmission in Africa. Reviewing the available evidence provides an opportunity to re-think transmission pathways, not only in Africa but also elsewhere, and also to pose questions. Does the predominance of human-to-human transmission in Africa reflect a relative absence of zoonotic C. parvum in African livestock? Are Africans less susceptible to zoonotic Cryptosporidium infection, perhaps resulting from early immunostimulation by C. hominis or due to inherent genetic traits? Is the African environment—in all its variety—simply more detrimental to oocyst survival? Will the so-called hypertransmissible subtypes, currently relatively rare in Africa, be introduced from Europe or elsewhere, and, if so, will they fade out or establish and spread? Our intention with this manuscript is not only to summarize and consolidate diverse data, thereby providing an overview of data gaps, but also to provide food for thought regarding transmission of a parasite that continues to have a considerable impact on both human and animal health.

An Unusual Cause of Watery Diarrhea

Question: A 54-year-old man presented to the emergency department with nausea, nonbloody nonbiliary emesis, left lower quadrant abdominal pain and profuse watery nonbloody diarrhea for the last 24 hours before presentation. He was unable to tolerate oral intake for the last few days before presentation. He denied recent travel, sick contacts, and consuming raw milk or meat. He denied smoking, drinking alcohol, or using illicit drugs. His vitals were remarkable for tachycardia at 106/min. He was afebrile.

S2162 Hemorrhagic Shock Following a Secretin Stimulating Test

INTRODUCTION: Zollinger-Ellison Syndrome (ZES) is a rare disorder resulting from inappropriate gastrin release, which causes acid hypersecretion and the development of peptic ulcer disease (PUD), severe gastroesophageal reflux, and diarrhea. Diagnosing ZES is challenging in the age of PPIs. Furthermore, discontinuing PPI therapy in patients with suspected ZES can be dangerous and even life-threatening. CASE DESCRIPTION/METHODS: A 44 y.o. male with a history of PUD presented for evaluation for ZES. Due to concern for ZES, a secretin-stimulating test was ordered. One week prior to his test he was instructed to stop his PPI and start Ranitidine 450 mg every 6 hours until 24 hours prior to the test. Immediately following the secretin-stimulating test he presented to the emergency room with nausea, vomiting, and profuse watery diarrhea. A pantoprazole infusion at 8 mg/ hr was started. Overnight he became tachycardic and developed about 400cc of hematemesis. His Hbg dropped from 10.3 g/dL to 7.7 g/dL. He subsequently developed hemorrhagic shock requiring intubation and transfer to the ICU. On EGD, he had a large clot in the second portion of the duodenum. He had hematin in the stomach and over 10 ulcers in the duodenum (Image 1). The pantoprazole infusion was increased to 12 mg/hr with no further recurrence of hemorrhage. The secretin stim test returned, confirming the diagnosis of ZES. This was followed up with an Octreotide scan, which revealed increased radiotracer near the second portion of the duodenum, confirming the location of the gastrinoma (Image 2). DISCUSSION: This case illustrates a rare complication of a patient with suspected ZES undergoing a secretin stimulating test. In patient’s with ZES, a secretin stimulating test causes a paradoxical gastrin response to secretin, likely from secretin receptors on tumor cells (Image 3). Furthermore, PPI withdrawal can cause rebound acid secretion, which can lead to exaggerated acid hypersecretion in patient's with ZES. Our patient had an exaggerated response to secretin leading to acid hypersecretion causing PUD, diarrhea, and hemorrhagic shock. Although complications from a secretin stimulating test are rare, in patients with prior UGIB and high suspicion for ZES, a secretin-stimulating test may need to be performed in a controlled hospitalized setting to minimize complication. This case further illustrates how the diagnosis of ZES has become difficult and whether we need to propose new diagnostic criteria to avoid complications in establishing a diagnosis.Figure 1.: Image 1. Large Clot and Multiple Ulcers (Yellow Arrows) in the Duodenum.Figure 2.: Image 2. Markedly increased radiotracer uptake in a soft tissue nodule medial to the second portion of the duodenum, suggestive of a neuroendocrine tumor (confirmed to be gastrinoma by surgical resection).Figure 3.: Image 3. A. In the antrum, exogenous secretin stimulates gastrin secretion directly and concomitantly inhibits gastrin secretion by stimulating somatostatin (SST) secretion, resulting in little or no gastrin release. B. In patients with ZES, because the gastrinoma does not contain functionally coupled SST cells, the effect of secretin is solely to stimulate gastrin secretion from the tumor.

Isolated Intestine Transplantation for Autoimmune Enteropathy: A Case Report

Autoimmune enteropathy is a rare disease characterized by chronic watery diarrhea, weight loss, and immune-mediated injury of the enterocolic mucosa. The clinicopathologic findings of this disease are variable, and timely diagnosis is challenging. It is usually managed medically. If medical management fails, surgical intervention is considered. This is a case report of a patient with autoimmune enteropathy mimicking collagenous enterocolitis. A 55-year-old man developed intestinal failure that manifested as profuse watery diarrhea, electrolyte disturbances, and weight loss. Initially, he was diagnosed with collagenous enterocolitis based on pathologic findings. Medical interventions were started, but the patient failed to show improvement. At 13 months after the onset of the disease, he was listed for isolated intestine transplantation (IITX) for intestinal failure. A healthy donor graft became available. IITX with chimney colostomy was performed. Based on the pathologic findings of the excised native small intestine, the patient was diagnosed with severe autoimmune enteropathy. The postoperative course was uneventful. By the third postoperative week, a full diet was tolerated and parenteral nutrition (PN) was weaned to end. He was discharged on postoperative day 34. Since discharge, he has been off PN, remaining on an enteral diet. This case is the first reported IITX performed on a patient with severe autoimmune enteropathy that was both curative and lifesaving. The present case confirms that IITX promptly restores gastrointestinal absorption in medically refractory autoimmune enteropathy. This observation provides clinicians with an effective treatment option in this challenging group of patients.

Сравнительная клинико-эпидемиологическая характеристика ротавирусной инфекции у детей раннего возраста

This article gives a comparative description of the clinical and epidemiological characteristics of rotavirus infection in children under 1 year and 1–3 years old. An analysis of 83 case histories of the examined children for rotavirus infection under the age of 3 years was carried out. Patients were divided into 2 groups: group 1 — children under 1-year-old (48 patients), group 2 — children from 1 to 3 years old (35 patients). As a result of the study, it was found that in children of the 1st group, rotavirus infection proceeded predominantly (Р˂0.01) in the form of severe enteritis (71.0%), in combination with bacterial intestinal infection (75.0%), with significant (P ˂0.05) frequent (31.3%) bloating due to profuse watery diarrhea. In children of this group in 4.0% of cases, the disease was fatal. In the vast majority (96.7%) of children of the 2nd group, rotavirus infection proceeded in the form of gastroenteritis, with almost the same ratio of moderate to severe forms (47.0, 50.0%). Due to large losses with repeated vomiting and loose stools, significantly (Р˂0.01) more often (53.3%) there was a decrease in urine output and an increase in creatinine level (40.0%).

Clinical Characteristics of Rotavirus-Induced Gastroenteritis in Infants

Abstract Rotavirus is the most common cause of acute infectious diarrhea in infants and young children up to the age of five. The disease is characterized by profuse watery diarrhea, vomiting and fever. The major complications of rotavirus gastroenteritis (RVGE) are dehydration, middle ear inflammation and upper respiratory tract infection. The basis of treatment is compensation for fluid loss and administration of probiotics. The aim of this study was to analyze the clinical characteristics of rotavirus gastroenteritis in infants. The study was conducted by the type of retrospective-prospective clinical study on infants with rotavirus gastroenteritis diagnosed on the basis of a positive Rotalex test (Orion Diagnostica Finland) and exclusion of other etiological factors at the University Children's Clinic in Belgrade, from April 2005 to December 2010. In addition to the detailed medical history and clinical examination, relevant laboratory analyzes were performed in all patients. Descriptive and analytical statistical methods were applied in the study. Among the descriptive methods, we used grouping, tabulation, graphing, calculating measures of central tendency, calculating measures of variability and calculating relative numbers. Of the analytical statistical methods, distribution normality testing, χ2 test, Mann-Whitney U test and T test were used. Statistical significance will be taken to mean p &lt; 0.05. The average infant mortality was 6.7 ± 3.7 months. All respondents were divided into two groups according to the age. The first group consisted of infants aged 0 to 5 months (46%), the second group consisted of infants aged 6 to 12 months (54%). The incidence of aqueous diarrhea (100%), vomiting (84%) and fever (74%) in infants suffering from rotavirus gastroenteritis was analyzed. The significance of the age on the symptomatology of rotavirus gastroenteritis as well as on the importance of using probiotics has been demonstrated.

A diarrhoeal blast from the past

Introduction: Diarrhoea is a common presentation in travellers. This case highlights the importance of providing the microbiology laboratory with necessary clinical information so that special media can be inoculated in order to establish a prompt diagnosis. Case Report: A 29 year-old male was admitted in Glasgow, UK with a 24 hour history of profuse watery diarrhoea. He was travelling from Mumbai, India. He reported no relevant sick or healthcare contacts. On admission he was dehydrated, tachycardic, and hypotensive. Blood testing revealed normal electrolytes but lactic acidosis, a severe AKI, neutrophilia, and raised CRP. Treatment was initiated with IV fluids, empirical IV ceftriaxone and azithromycin. Urine, faeces and blood cultures were collected and rectal screening for CPE was performed. More than 6L of diarrhoea was passed in the first 12 hours. Over the subsequent 48 hours diarrhoea continued while urine output and biochemistry normalised with IV fluids. Yellow colonies were grown from faecal cultures on TCSB agar. Gram stain revealed short, ‘comma-shaped’ gram negative aerobic rods. These were identified asVibrio choleraeusing MALDI-TOF and later confirmed to be serotype 01 El Tor. Rectal swabs returned positive for NDM-1 producing Escherichia coli. By the third day his diarrhoea resolved, antibiotics and IV fluids were discontinued and he was discharged. Conclusion: This case highlights the challenge of managing V. cholerae infection in a traveller. Cholera should be considered in the differential diagnosis of diarrhoea in any traveller and specific laboratory testing is required to make a positive diagnosis.

Electrolytes, Serum biochemical and Acid-Base Disturbances in Dogs with Foul-Smelling Bloody Diarrhoea

Metabolic alkalosis is an electrolyte abnormality accompanied by an elevation in bicarbonate ion concentration in blood and a rise in blood pH. This study aims to determine the serum concentration of electrolytes and levels of some biochemical parameters in dogs presented with profuse foul-smelling bloody watery diarrhoea. From October 2018 to February 2019, 60 client-owned dogs were presented at the University of Nigeria Veterinary Teaching Hospital (UNVTH) for vaccination, treatment and regular deworming. Five (5) out of 60 dogs had profuse foul-smelling watery diarrhoea and were sampled. A full history and physical examinations were undertaken for the sampled dogs. Clinical signs such as profuse foul-smelling bloody diarrhoea, vomiting, anorexia, weakness, dehydration, lethargy was observed in the affected dogs. Three dogs were 4 months old while two dogs are adults. Blood samples (2 ml) were collected from the cephalic vein of dogs with the above presentation, and sera were harvested for serum biochemical analysis. Standard procedures were followed in all the serum biochemistry determinations. The most common electrolyte and serum biochemical abnormalities in 5 dogs with profuse foul-smelling bloody watery diarrhoea were hypokalemia (100%), increased serum bicarbonate level (100%), hyponatremia (75%), and hypoglobulinemia (100%). Hypochloremia occurred in 20% of the cases, while hypoproteinemia, hypoglobulinemia, and low serum creatinine levels were recorded in 100% of the cases. Increased urea level was observed in 40% of the affected dogs. Our study demonstrated that all affected dogs developed hypokalemic metabolic alkalosis following loss of potassium through the gastrointestinal tract consequent upon severe watery diarrhoea.

Neuropathology mediated through caspase dependent extrinsic pathway in goat kids naturally infected with PPRV

Peste des petits ruminant (PPR), a highly contagious viral disease of small ruminants, is characterized by erosive stomatitis and pneumo-enteritis. However, its neurovirulence potential as observed with other morbilliviruses has not been fully investigated. The present study describes the neuropathological alterations induced by PPR virus through apoptotic pathway. A total number of 12 carcasses of local breed goat kids of either sex were received for postmortem examination. The clinical history was described as symptoms of mucopurulent nasal discharge, high to low grade fever, erosive stomatitis, dyspnoea and profuse watery diarrhoea followed by mortality of 35 goat kids within a week. The pathoanatomical lesions and immunohistochemical demonstration of PPRV antigen in lungs, intestine, spleen and lymph nodes confirmed PPR disease in goats. Grossly, five brain specimens showed moderate to severe leptomeningeal congestion during necropsy. Microscopically, brain sections showed leptomeningitis and nonsuppurative encephalitis characterized by vascular congestion, haemorrhages in the parenchyma, perivascular cuffing with mild to moderate mononuclear cells (mainly lymphocytes and few macrophages), focal to diffuse microgliosis, neuronal degeneration, satellitosis and neuronophagia. Immunolabelling of viral antigen was observed in the cytoplasm of neurons and glial cells. The RT-PCR amplification of N gene fragment also confirmed the presence of PPRV in the brain. The strong immunoreactivity of Caspase-3, Caspase-8 and comparatively lower expression of caspase-9 along with the absence of any reactivity for Apaf-1 antigen in the brain sections indicated the role of caspase dependent extrinsic pathway in inducing neuropathological changes. The presence of apoptotic neurons in the brain by TUNEL assay further confirmed the apoptosis and strong immunoreactivity of iNOS in neurons which suggested the generation of oxidative stress, that might have induced the apoptosis. The overall findings confirm the neurovirulence potential of PPR virus, via the extrinsic pathway of apoptosis, in natural cases of PPR disease in goat kids.

1408 A Tail of Acute Diarrhea

INTRODUCTION: VIPomas are neuroendocrine neoplasms arising from the pancreas in 90% of the cases reported, while the remaining 10% occur in other tissues of neural crest origin. The symptoms found are secondary to an excessive secretion of vasoactive intestinal peptide (VIP) including profuse watery diarrhea, dehydration, hypokalemia and hypoclorhydria. VIPomas are classically slow-growing, and previously reported cases consistently describe chronic diarrhea and a slowly progressing constellation of associated symptoms. We present a case of acute onset of secretory diarrhea secondary to a VIPoma. CASE DESCRIPTION/METHODS: The patient is a 62 y/o F with PMHx of HTN who presented to the ED w/complaints of abdominal pain, diarrhea, nausea and vomiting for approximately 3 days. Patient reported she was having 5-6 episodes of large volume, pale colored diarrhea. She denied any weight loss, change in diet, recent travel, blood in the stool, foul smell or bulky stool. She was initially found to be hypotensive BP 85/45, MAP 58, HR 88. Labs revealed K+ 3.1 meq/L, HCO3 was 16 meq/L, she had an AGMA measured at 15, and AKI with BUN: Cr 52:3.60 mg/dl respectively. On exam of the stool she was noted to have a stool osmolar gap of -14. Given no obvious underlying cause for these findings she underwent CT A/P which revealed a 7.8 × 6 cm mass contiguous w/both body/tail of the pancreas and posterior wall of the stomach, with no other sites of metastasis. EUS/FNA was done and pathology returned as NET type 1. VIP levels were subsequently sent and were elevated at 1385.8 pg/mL. She was started on octreotide 50 mcg TID with significant improvement in her diarrhea. She underwent surgery with distal pancreatectomy and splenectomy. Pathology confirmed the presence of a grade 2, stage T3 well differentiated NET. She had an uneventful recovery and was discharged home. She continues to be asymptomatic several weeks after surgery. DISCUSSION: Pancreatic VIPoma was first described in 1958 by Verner and Morrison in a patient with chronic refractory diarrhea and hypokalemia. VIPoma is very rare with an estimated incidence of 0.05-0.2 cases per million people. Acute diarrhea resulting from a VIPoma is rare event in an already rare malignancy. Our patient presented with acute secretory diarrhea proven by a stool osmolar gap less than 50, which resulted in acute kidney injury. Her diarrhea, secondary to VIPoma responded well to octreotide. VIPomas are classically rare tumors, but our specific case presents an even more rare presentation.

Establishment and application of isothermal multiple-self-matching-initiated amplification (IMSA) in detecting Type II heat-labile enterotoxin of Escherichia coli.

Enterotoxigenic Escherichia coli (ETEC) constitutes a major cause of diarrhea in young children and animals, particularly in poor regions of the world, as well the traveler’s diarrhea in adult individuals. Type II heat-labile enterotoxin (LT-II) from ETEC can cause profuse watery diarrhea, posing a potential threat to public health and animal husbandry. In the present study, isothermal multiple-self-matching-initiated amplification (IMSA) was established to rapidly detect LT-II producing ETEC. The specificity and sensitivity were assessed, and clinical samples were tested. The established IMSA method had good specificity for the detection of LT-II gene with a limit of detection of 25 CFU/mL, i.e. 2 times higher than that of real-time PCR and other two isothermal amplifications (loop-mediated isothermal amplification, LAMP and cross-primer isothermal amplification, CPA). Meanwhile, in 103 clinical Escherichia coli strains isolated from diarrhea samples, 9 strains with LT-II+ gene were detected (8.73%), corroborating real-time PCR, LAMP and CPA data. Therefore, the IMSA technology applied for the detection of LT-II producing ETEC has a good application prospect for screening clinical samples in primary medical units or common laboratories.

A 10-year-old boy presented with recurrent episodes of diarrhea, low grade, irregular fever and severe wasting

This article has no abstract. The first 100 words appear below: A 10-year old boy, the only issue of his deceased parents, was admitted to the department for the management of recurrent episodes of diarrhea and severe wasting for 2.5 months, low grade, irregular fever with evening rise of temperature, anorexia and repeated attack of skin blister for the last 1 year. The patient complained of chronic, painless, non-bloody, profuse watery diarrhea with a weight loss of 10 kg (decrease to 18 kg from 28 kg prior to illness). He also complained of cough for the last seven days. His father was a driver and died at his 1 year of age due to an unknown disease.

AphA is a master regulator of natural competence in Vibrio cholerae

Vibrio cholerae is the etiological agent of cholera, a disease affecting 4.3 million people each year (WHO, 2015). The symptoms of cholera include profuse watery diarrhoea and vomiting, leading to coma and death in serious cases. The El Tor biotype of V. cholerae is globally predominant, and the success of this biotype to cause disease is thought to be due, in part, to the ability of the organism to successfully colonise two different environments; i) marine and brackish coastal waters where V. cholerae forms biofilms on the chitinous surfaces of shellfish, and ii) the human intestine. When bound to chitinous surfaces V. cholerae expresses genes required for biofilm formation, chitin utilisation and natural competence. Conversely, within the human host, V. cholerae switches on the expression of virulence genes. The transcription factor AphA was discovered as a regulator of genes encoding the toxin co-regulated pilus (TCP) of V. cholerae. It is also known that AphA is active when V. cholerae populations have a low cell density. Hence, AphA is generally considered a regulator of virulence and quorum sensing. We have mapped DNA binding by AphA across the entire V. cholerae genome. The majority of AphA target genes encode cell surface and cell envelope proteins. Unexpectedly, we show that AphA also targets key gene clusters within the natural competence regulon of V. cholerae. Using biochemistry and genetics we show that AphA is a master repressor of natural competence and acts to antagonise transcription activation by the cyclic-AMP receptor protein.

Accidental Ricinus Communis Oil Cake Intoxication in a Dairy Cow

The aim of the study to report a case of spontaneous toxicity in a 5 year old Crossbred Jersey cow with a history of accidental ingestion of Ricinus communis oil cake during the month of November 2017. The animal had anorexia and profuse watery yellowish mucoid diarrhoea. On clinical examination the animal showed dullness and depression, congested conjunctival mucous membrane, tachycardia and doughy rumen with absence of rumen motility. The whole blood and sera samples were collected for haemato-biochemical analysis. The haematological values showed mild haemoconcentration with normocytic normochromic anaemia. There was no abnormality in biochemical values. Electrocardiography revealed sinus tachycardia. On ultrasound examination the liver and kidney showed normal contour and intestinal loops showed increased wall thickness without distension. The animal was treated with activated charcoal, egg white, fluid therapy, purgatives, antioxidants (Ascorbic acid) and low dose of sodium bicarbonate. The animal recovered uneventfully after three days of treatment. Recovery is generally less common in ricin poisonings.

Ulcerative stomatitis associated with ingestion of broomsedge hay in a horse

An adult mare presented acutely down in the pasture on January 21, 2018. On arrival at the farm, the mare was found recumbent with a heart rate of 60 beats...

Severe falciparum malaria with hypophosphataemia and presumed hypophosphatemia induced rhabdomyolysis: a case report

Malaria is eliminated from Sri Lanka, yet cases contracted overseas are still encountered in the country. It is therefore important to be vigilant of possible complications of severe malaria. We report a 31-year-old sailor (Sri Lankan national) with a recent travel history to West Africa who presented with an acute febrile illness of seven days duration. He had high fever, myalgia, drowsiness as well as profuse watery diarrhea. Clinical examination revealed a febrile patient with GCS 15 with no features of meningism. He was icteric with right hypochondrial tenderness. Investigations showed hemolysis. Microscopy and rapid diagnostic assays revealed Plasmodium falciparum infection. He was started on IV artesunate followed by artemisinin based combination therapy orally to which he responded. On day 4 he developed evidence of rhabdomyolysis with low serum phosphate and normal urine phosphate levels. Hypophosphatemia was considered to be the driving factor for rhabdomyolysis, and phosphate replacement was done for which the patient responded and was discharged on day 10 fully recovered.